Vitamin D binding protein-macrophage activating factor (DBP-maf) inhibits angiogenesis and tumor growth in mice
Vitamin D binding protein-macrophage activating factor (DBP-maf) inhibits angiogenesis and tumor growth in mice
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DOI：
10.1016/s1476-5586(03)80015-5
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发表时间：
2003-01-01
期刊：
影响因子：
4.8
通讯作者：
Pirie-Shepherd, S
中科院分区：
文献类型：
--
作者：
Kisker, O;Onizuka, S;Pirie-Shepherd, S
我们分离了一种选择性脱糖形式的维生素D结合蛋白(DBP-MAF)，它是由人胰腺癌细胞株从系统可用的DBP中产生的。DBP-MAF对血管内皮细胞具有抗增殖作用，在绒毛尿囊膜实验中具有抗血管生成作用。DBP-MAF每日给药能有效抑制免疫缺陷小鼠人胰腺癌的生长(T/C=0.09)。在较高剂量下，DBP-MAF可导致肿瘤消退。组织学检查显示，与未治疗的肿瘤相比，经治疗的肿瘤有更多的巨噬细胞渗入，微血管密度降低，细胞凋亡水平增加。综上所述，这些数据表明，DBP-MAF是一种抗血管生成分子，可以直接作用于内皮细胞，也可以刺激巨噬细胞攻击不断增长的恶性肿瘤的内皮细胞和肿瘤细胞。
We have isolated a selectively deglycosylated form of vitamin D binding protein (DBP-maf) generated from systemically available DBP by a human pancreatic cancer cell line. DBP-maf is anti proliferative for endothelial cells and antiangiogenic in the chorioallantoic membrane assay. DBP-maf administered daily was able to potently inhibit the growth of human pancreatic cancer in immune compromised mice (T/C=0.09). At higher doses, DBP-maf caused tumor regression. Histological examination revealed that treated tumors had a higher number of infiltrating macrophages as well as reduced microvessel density, and increased levels of apoptosis relative to untreated tumors. Taken together, these data suggest that DBP-maf is an antiangiogenic molecule that can act directly on endothelium as well as stimulate macrophages to attack both the endothelial and tumor cell compartment of a growing malignancy.